Hyperactivation of AKT, due to gain-of-function mutations or amplification of oncogenes (receptor tyrosine kinases and PI3K) or inactivation of tumor suppressor genes (PTEN, INPP4B, and PHLPP), is one of the most common molecular perturbations in cancer and promotes malignant phenotypes associated with tumor initiation and progression.118 Thus, AKT is an attractive therapeutic target. This evidence concerns the gene PHLPP1 and neoplasm.